Most of the iron in a mammalian body is complexed with various protein
s. Moreover, in response to infection, iron availability is reduced in
both extracellular and intracellular compartments. Bacteria need iron
for growth and successful bacterial pathogens have therefore evolved
to compete successfully for iron in the highly iron-stressed environme
nt of the host's tissues and body fluids. Several strategies have been
identified among pathogenic bacteria, including reduction of ferric t
o ferrous iron, occupation of intracellular niches, utilisation of hos
t iron compounds, and production of siderophores. While direct evidenc
e that high affinity mechanisms for iron acquisition function as bacte
rial virulence determinants has been provided in only a small number o
f cases, it is likely that many if not all such systems play a central
role in the pathogenesis of infection.